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Explaining Reflex Sympathetic Dystrophy
Arch Neurol. 1999;56:521-522.
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THE ARTICLE by Wasner and colleagues1 clearly demonstrates a complete functional loss of cutaneous sympathetic vasoconstrictor activity in a very early stage of reflex sympathetic dystrophy/complex regional pain syndrome type I (RSD/CRPS I) that returns with clinical recovery. They also present compelling evidence that this autonomic dysfunction is located within the central nervous system. This elegant clinical study of 1 patient and 2 control subjects addresses the role of the sympathetic nervous system in the early stages of RSD/CRPS I by measuring cutaneous blood flow (laser Doppler flowmetry) under phasic and tonic conditions that parallels vasoconstrictor innervation. Two weeks after the onset of RSD/CRPS I, the skin temperature of the patient's affected extremity was higher than that measured on the contralateral side at room temperature and during controlled thermoregulation, which demonstrated maximal vasodilation. Phasic stimulation (deep respiration) that causes cutaneous vasoconstriction and tonic cutaneous vasoconstriction (controlled body hypothermia) did not . . . [Full Text of this Article]
RELATED ARTICLE
Vascular Abnormalities in Acute Reflex Sympathetic Dystrophy (CRPS I): Complete Inhibition of Sympathetic Nerve Activity With Recovery
Gunnar Wasner, Klaus Heckmann, Christoph Maier, and Ralf Baron
Arch Neurol. 1999;56(5):613-620.
ABSTRACT
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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
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Neuropathic Central Pain: Epidemiology, Etiology, and Treatment Options
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Arch Neurol 2001;58:1547-1550.
ABSTRACT
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Nosological entities?: Reflex sympathetic dystrophy
Schott
J. Neurol. Neurosurg. Psychiatry 2001;71:291-295.
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